A SAFER way to reduce the risk of heart attacks and strokes is a step closer thanks to the identification of a protein that controls the 鈥渟tickiness鈥� of blood.
When a blood vessel wall is damaged, cells that circulate in the blood called platelets send out tiny sticky 鈥渁rms鈥� that latch onto other platelets to form a blood clot (see photo, above). The arms also 鈥済lue鈥� the clot to the injury, stemming the bleeding. But sometimes clots block arteries supplying the heart or brain, causing heart attacks and strokes.
To investigate the process, , a British Heart Foundation researcher at the University of Birmingham, UK, and colleagues used engineered mice that lack CD148, a protein they suspected of switching on the formation of platelet arms.
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Platelets from the blood of these mice were slow to respond to injury, sent out fewer arms, and formed smaller clots compared with platelets taken from normal mice (Blood, ). Crucially, the lack of CD148 did not cause dangerous bleeding. This is probably because absence of CD148 stops just one of the chemical pathways leading to clot formation, whereas existing blood thinners like aspirin carry the risk of bleeding because they block all pathways.
CD148 blockers could make safer blood thinners, while boosting CD148 might be an idea in those likely to get injured, says Senis.